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Effect of endothelin-1 in man—impact on basal and stimulated concentrations of luteinizing hormone, follicle-stimulating hormone, thyrotropin, growth hormone, corticotropin, and prolactin with and without pretreatment with nifedipine
In healthy men, intravenous (IV) endothelin-1 suppresses the growth hormone (GH)-releasing hormone (GHRH)-stimulated increase in GH and prolactin (PRL) and augments corticotropin (ACTH)-releasing factor (CRF)-stimulated secretion of ACTH. Since some actions of endothelin-1 on pituitary function in v...
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Published in: | Metabolism, clinical and experimental clinical and experimental, 1996-05, Vol.45 (5), p.658-661 |
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Main Author: | |
Format: | Article |
Language: | English |
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Online Access: | Get full text |
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Summary: | In healthy men, intravenous (IV) endothelin-1 suppresses the growth hormone (GH)-releasing hormone (GHRH)-stimulated increase in GH and prolactin (PRL) and augments corticotropin (ACTH)-releasing factor (CRF)-stimulated secretion of ACTH. Since some actions of endothelin-1 on pituitary function in vitro are antagonized by calcium channel antagonists, we have studied the effect of pretreatment with oral nifedipine (10 mg, given before infusion of endothelin-1 or vehicle) on basal and stimulated concentrations of pituitary hormones in a group of healthy men (N = 6). The augmentative effect of endothelin-1 on CRF-induced ACTH secretion (
P < .05) was counteracted by pretreatment with nidefipine. Pretreatment with nifedipine further inhibited (
P < .01) the GHRH-induced increase in plasma concentrations of GH (
P < .05), which, in keeping with previous data, had already been reduced by IV endothelin-1 alone (
P < .05). Thus, both endothelin-1 and nifedipine influence pituitary hormone secretion in healthy man. However, nifedipine does not ubiquitously counteract the effects of endothelin-1 since it enhances some of its actions on the pituitary and diminishes others. Endothelin-1 may therefore influence pituitary function by mechanisms other than activation of calcium channels alone. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1016/S0026-0495(96)90039-6 |